Given that 53BP1 shifts the balance of the repair of DNA double‐strand breaks towards the more error‐prone pathway of nonhomologous end‐joining, at the expense of the more accurate homologous recombination (Lord and Ashworth, 2012) (Jackson and Bartek, 2009), such altered balance among the key cellular pathways of DNA break repair would then likely fuel the chromosomal instability of the cancer cells over time, consistent with the high degree of genomic instability known to occur in medulloblastomas, among other malignancies. The gene discussed is TP53BP1; the disease is cancer.